Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 48, Pages 10858-10867Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1022-04.2004
Keywords
calcium/calmodulin; memory; consolidation; transgenic; CREB; tetracycline
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Funding
- NIMH NIH HHS [5R01MH057368-06, R01 MH057368] Funding Source: Medline
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The neuronal response to a Ca2+ stimulus is a complex process involving direct Ca2+/calmodulin (CaM) actions as well as secondary activation of multiple signaling pathways such as cAMP and ERK(extracellular signal-regulated kinase). These signals can act in both the cytoplasm and the nucleus to control gene expression. To dissect the role of nuclear from cytoplasmic Ca2+/CaM signaling in memory formation, we generated transgenic mice that express a dominant inhibitor of Ca2+/CaM selectively in the nuclei of forebrain neurons and only after the animals reach adulthood. These mice showed diminished neuronal activity-induced phosphorylation of cAMP response element-binding protein, reduced expression of activity-induced genes, altered maximum levels of hippocampal long-term potentiation, and severely impaired formation of long-term, but not short-term, memory. Our results demonstrate that nuclear Ca2+/CaM signaling plays a critical role in memory consolidation in the mouse.
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